Lab Value Calculator
A low albumin hides a raised anion gap — 34% of apparently-normal gaps correct to raised, and none ever correct back.
A study aid, not a diagnostic tool. Every correction here is a regression fitted to a population, not a measurement of anyone. Reference ranges differ between laboratories and analysers — the anion gap normal range in particular shifted when ion-selective electrodes replaced older methods. Nothing here knows anything about a patient, and it never replaces clinical judgement.
What the albumin does to both corrections
Corrected sodium — two published factors
A low albumin hides an acidosis
Albumin is itself an unmeasured anion, so a low albumin removes anions from the gap and conceals a raised one. The correction adds 2.5 mmol/L for every g/dL below 4.0 — and below that reference it can only ever add. Across a sweep of plausible chemistries, 34 per cent of apparently-normal measured gaps correct to raised, and not one raised gap corrects back to normal. Since hypoalbuminaemia is near-universal in the critically ill, that is a bias pointing straight at the population where a concealed acidosis matters most.
The calcium correction does even more work relative to what it is correcting. The reference interval is only 2.0 mg/dL wide, while at an albumin of 2.0 the correction adds 1.6 — eighty per cent of the whole range — and at 1.5 it adds the entire range. A measured 7.6, clearly low, becomes 9.2, comfortably normal, on the strength of the albumin alone. A formula that can move a result clean across its own reference interval is carrying more weight than a 1970s linear regression deserves, and it performs worst in exactly the critically ill patients it gets used on. Where the answer matters, ionised calcium is measured directly.
The sodium correction has a different problem: there are two published factors and they disagree by fifty per cent. Katz gives 1.6 mmol/L per 100 mg/dL of glucose and Hillier gives 2.4 — a 7.2 mmol/L difference at a glucose of 1000, and opposite sides of the hyponatraemia threshold in nine per cent of plausible cases. That is a genuine unresolved argument in the literature rather than one formula being wrong, so both are shown here rather than one being picked for you.
How to use
- Enter the chemistry panel; albumin drives two of the corrections.
- Read the corrected anion gap, not just the measured one.
- Compare both published sodium factors before trusting either.
- Add a measured osmolality to get an osmolal gap.
Frequently asked questions
Why does the anion gap need correcting for albumin?
Because albumin is itself an unmeasured anion, and the gap is made of unmeasured anions. A low albumin removes some of them, so the gap reads lower than the acid-base picture warrants. The usual correction adds 2.5 mmol/L for every g/dL of albumin below 4.0, and below that reference it can only ever add.
How often does the albumin correction change the answer?
Across a sweep of plausible chemistries, 34 per cent of apparently-normal measured gaps correct to raised — and not one raised gap corrects back to normal. The bias runs in a single direction below the reference albumin, and since hypoalbuminaemia is near-universal in the critically ill, it points straight at the patients where a concealed acidosis matters most.
What is a normal anion gap?
Conventionally 8 to 12 mmol/L, but this is one of the numbers that genuinely varies by laboratory. The range shifted downward when ion-selective electrodes replaced older methods of measuring chloride, so some laboratories report a normal range nearer 3 to 11. A textbook figure may not match the one your laboratory uses, and the laboratory range is the one that applies.
How does corrected calcium work?
It adds 0.8 mg/dL for every g/dL of albumin below 4.0, on the reasoning that roughly half of serum calcium is protein-bound and a low albumin therefore lowers the total without lowering the physiologically active ionised fraction. It is a linear regression from the 1970s rather than a measurement of binding.
How much does the calcium correction actually move things?
More than the entire reference interval, at low albumin. The normal range is only 2.0 mg/dL wide, while at an albumin of 2.0 the correction adds 1.6 — eighty per cent of it — and at 1.5 it adds the whole range. A measured 7.6, clearly low, becomes 9.2, comfortably normal, on the strength of the albumin alone.
Should I trust corrected calcium?
For screening, it is a reasonable convenience. Where the answer matters, ionised calcium is measured directly instead, because the correction is a population regression that performs worst in exactly the critically ill patients it is most often applied to. A formula that can move a result clean across its own reference interval deserves that scepticism.
Why does sodium need correcting in hyperglycaemia?
Because glucose is osmotically active and draws water out of cells into the blood, diluting the sodium. The measured sodium is therefore lower than the sodium the patient will have once the glucose is corrected, and the correction estimates that final value — which is what determines how the sodium should be managed.
Which sodium correction factor is right, 1.6 or 2.4?
This is genuinely unresolved rather than one of them being wrong. Katz derived 1.6 in 1973 and it remains the most widely taught; Hillier derived 2.4 from an experimental study in 1999, and it is better supported at very high glucose. They differ by fifty per cent, which is why both are shown here rather than one being chosen for you.
Does the choice of sodium factor change the verdict?
In about nine per cent of plausible cases, yes — the two land on opposite sides of the 135 hyponatraemia threshold. At a glucose of 1000 they differ by 7.2 mmol/L, which is a clinically substantial gap. At a mildly raised glucose the two barely differ, which is why the disagreement stays invisible until it matters.
What is the osmolal gap for?
Finding an unmeasured osmole — chiefly a toxic alcohol such as methanol or ethylene glycol. It is the difference between measured osmolality and the value calculated from sodium, glucose and urea, and a gap above about 10 raises the question. A normal gap does not exclude poisoning late in its course, once the alcohol has been metabolised into acids that the anion gap sees instead.
Why is sodium doubled in the osmolality calculation?
To account for the anions that accompany it, chiefly chloride and bicarbonate. That doubling makes sodium dominate the estimate: one mmol/L of sodium moves the calculated osmolality by 2 mOsm/kg, the same as about 36 mg/dL of glucose. A small sodium error therefore does more damage to an osmolal gap than a large glucose one.
Can I use these calculations clinically?
No. This is a study and teaching aid for people learning them. Every correction here is a regression fitted to a population rather than a measurement of anyone, each was derived in a different population, and each fails somewhere — usually in the sickest patients, because they are furthest from the group the formula was fitted to.
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